Immunoglobulin E, the potential accelerator of comorbid psoriasis and atherosclerosis

Immunoglobulin (Ig) E is a key mediator in the induction and maintenance of allergic inflammation, characterized by a Th2-dominated immune response. Recently epidemiological studies have showed that elevated serum total IgE levels or an increased abundance of mast cells (MCs) at the lesion site are observed in psoriatic patients with cardiovascular diseases (CVD), such as atherosclerosis. Although the underlying mechanisms by which IgE synergizing with MCs in promoting these chronic immune-inflammatory diseases remain unclear, the interleukin (IL)-23/IL-17 axis appears to play a crucial role in comorbidity of psoriasis and atherosclerosis. High IgE production may result from IL-17A response, further exacerbating inflammatory pathways involved in both psoriasis and atherosclerosis. This review explores the possible mechanisms of IgE in these comorbid conditions, reinforcing the rationale for IL-17A targeted biologics in the treatment of psoriasis and atherosclerosis comorbidity. Additionally, IgE is proposed as a potential therapeutic target for alleviating patients suffering from these comorbidity conditions.